Vascular role of vasopressin in the presence and absence of influence from angiotensin II or α-adrenergic system

Abstract

The effects of a vasopressin (AVP) pressor antagonist, d(CH₂)₅Tyr(Me)AVP, on mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO), and the distribution of CO were investigated by the microsphere technique in three groups of pentobarbital anesthetized rats: intact (I), saralasin pretreated (II), and phentolamine pretreated (III). Saralasin and phentolamine were infused intravenously to inactivate the renin–angiotensin and α-adrenergic systems, respectively. The AVP antagonist decreased MAP and TPR in all groups and it caused a greater depressor effect in groups II and III than in group I. In group I, AVP antagonist increased blood flow (BF) to the stomach and skin. In group II, AVP antagonist increased BF to the muscle and skin. In group III, AVP antagonist markedly increased BF to the muscle. Therefore, the degree of vasoconstrictor influence exerted by AVP in different vascular beds varies depending on endogenous vasomotor tone from the renin–angiotensin and (or) sympathetic nervous systems.